PDF(Pubmed)
Abstract：
UNASSIGNED: To investigate the possible molecular mechanism of miR-194-5p/PRC1/Wnt/β-catenin signaling axis that regulates the invasive metastatic ability and radiotherapy sensitivity of esophageal squamous cell carcinoma (ESCC) cells.
UNASSIGNED: ESCC-related differentially expressed miRNAs were identified by microarray analysis, followed by the identification of a putative target. The targeting relationship between miR-194-5p and PRC1 was assayed. A series of mimic and shRNA were transfected into ESCC cells to find out the mechanism of miR-194-5p in ESCC by regulating PRC1 through Wnt/β-catenin signaling pathway and their effect on cell proliferation, migration, invasion, and radiosensitivity as well as xenograft tumor growth and metastasis in nude mice.
UNASSIGNED: We demonstrated low miR-194-5p expression and high PRC1 expression in ESCC tissues and cells. PRC1 was confirmed as a putative target for miR-194-5p. High miR-194-5p or silenced PRC1 enhanced ESCC cell radiosensitivity but reduced proliferation, invasion, and migration via PRC1 through modulation of the Wnt/β-catenin signaling pathway. Animal experiments also validated that overexpression of miR-194-5p suppressed tumorigenesis and in vivo metastasis in nude mice.Conclusion: miR-194-5p can inhibit the Wnt/β-catenin signaling pathway through down-regulation of the PRC1 gene, thereby enhancing the sensitivity of ESCC cells to radiotherapy and attenuating the invasion and metastasis ability of ESCC cells.
UNASSIGNED: ESCC-related differentially expressed miRNAs were identified by microarray analysis, followed by the identification of a putative target. The targeting relationship between miR-194-5p and PRC1 was assayed. A series of mimic and shRNA were transfected into ESCC cells to find out the mechanism of miR-194-5p in ESCC by regulating PRC1 through Wnt/β-catenin signaling pathway and their effect on cell proliferation, migration, invasion, and radiosensitivity as well as xenograft tumor growth and metastasis in nude mice.
UNASSIGNED: We demonstrated low miR-194-5p expression and high PRC1 expression in ESCC tissues and cells. PRC1 was confirmed as a putative target for miR-194-5p. High miR-194-5p or silenced PRC1 enhanced ESCC cell radiosensitivity but reduced proliferation, invasion, and migration via PRC1 through modulation of the Wnt/β-catenin signaling pathway. Animal experiments also validated that overexpression of miR-194-5p suppressed tumorigenesis and in vivo metastasis in nude mice.Conclusion: miR-194-5p can inhibit the Wnt/β-catenin signaling pathway through down-regulation of the PRC1 gene, thereby enhancing the sensitivity of ESCC cells to radiotherapy and attenuating the invasion and metastasis ability of ESCC cells.
摘要：
■探讨miR-194-5p/PRC1/Wnt/β-catenin信号轴调控食管鳞状细胞癌(ESCC)细胞侵袭转移能力和放疗敏感性的可能分子机制。
■通过微阵列分析鉴定ESCC相关差异表达的miRNA，然后确定一个假定的目标。检测miR-194-5p与PRC1的靶向关系。将一系列模拟物和shRNA转染到ESCC细胞中，以了解miR-194-5p通过Wnt/β-catenin信号通路调控PRC1在ESCC中的作用机制及其对细胞增殖的影响。迁移,入侵,和放射敏感性以及裸鼠中异种移植肿瘤的生长和转移。
■我们证明了在ESCC组织和细胞中miR-194-5p的低表达和PRC1的高表达。PRC1被证实为miR-194-5p的推定靶标。高miR-194-5p或沉默的PRC1增强了ESCC细胞的放射敏感性，但降低了增殖，入侵,并通过调节Wnt/β-catenin信号通路通过PRC1迁移。动物实验还证实miR-194-5p的过表达抑制裸鼠中的肿瘤发生和体内转移。结论:miR-194-5p可通过下调PRC1基因抑制Wnt/β-catenin信号通路,从而增强ESCC细胞对放疗的敏感性并减弱ESCC细胞的侵袭和转移能力。
■通过微阵列分析鉴定ESCC相关差异表达的miRNA，然后确定一个假定的目标。检测miR-194-5p与PRC1的靶向关系。将一系列模拟物和shRNA转染到ESCC细胞中，以了解miR-194-5p通过Wnt/β-catenin信号通路调控PRC1在ESCC中的作用机制及其对细胞增殖的影响。迁移,入侵,和放射敏感性以及裸鼠中异种移植肿瘤的生长和转移。
■我们证明了在ESCC组织和细胞中miR-194-5p的低表达和PRC1的高表达。PRC1被证实为miR-194-5p的推定靶标。高miR-194-5p或沉默的PRC1增强了ESCC细胞的放射敏感性，但降低了增殖，入侵,并通过调节Wnt/β-catenin信号通路通过PRC1迁移。动物实验还证实miR-194-5p的过表达抑制裸鼠中的肿瘤发生和体内转移。结论:miR-194-5p可通过下调PRC1基因抑制Wnt/β-catenin信号通路,从而增强ESCC细胞对放疗的敏感性并减弱ESCC细胞的侵袭和转移能力。
